Expression of the bile acid receptor FXR in Barrett's esophagus and enhancement of apoptosis by guggulsterone in vitro
2006

FXR and Apoptosis in Barrett's Esophagus

Sample size: 24 publication Evidence: moderate

Author Information

Author(s): De Gottardi Andrea, Dumonceau Jean-Marc, Bruttin Fabien, Vonlaufen Alain, Morard Isabelle, Spahr Laurent, Rubbia-Brandt Laura, Frossard Jean-Louis, Dinjens Winand NM, Rabinovitch Peter S, Hadengue Antoine

Primary Institution: University Hospital, Geneva, Switzerland

Hypothesis

FXR and VDR are expressed in the esophagus and may contribute to the regulation of apoptosis in intestinal metaplasia.

Conclusion

The bile acid receptor FXR is significantly overexpressed in Barrett's esophagus compared to normal mucosa, and guggulsterone treatment enhances apoptosis in Barrett's esophagus-derived cells.

Supporting Evidence

  • FXR expression was significantly higher in Barrett's esophagus compared to normal esophagus.
  • Guggulsterone treatment increased apoptosis in Barrett's esophagus-derived cells.
  • VDR expression did not significantly differ between groups.

Takeaway

This study found that a receptor called FXR is more active in Barrett's esophagus, and a substance called guggulsterone can help kill bad cells in this condition.

Methodology

The study measured FXR and VDR expression in esophageal biopsies and cell lines using Q-PCR and immunohistochemistry, and assessed apoptosis in cell cultures treated with guggulsterone.

Limitations

Cell cultures were continuously exposed to guggulsterone at a neutral pH, which may not reflect physiological conditions.

Participant Demographics

{"Normal esophagus":{"n":6,"age":"55 ± 7","male_percentage":17},"Reflux esophagitis":{"n":6,"age":"50 ± 9","male_percentage":50},"Barrett's esophagus":{"n":6,"age":"78 ± 3","male_percentage":67},"Esophagus adenocarcinoma":{"n":6,"age":"79 ± 8","male_percentage":67}}

Statistical Information

P-Value

7·10-5

Statistical Significance

p<0.05

Digital Object Identifier (DOI)

10.1186/1476-4598-5-48

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